SESSION TITLE: Critical Care Global Case Reports
SESSION TYPE: Global Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: Acute respiratory distress syndrome (ARDS) is the onset of lung injury within 7 days of some defined event (trauma, infection, surgery, or reaction) with bilateral opacities that cannot be fully explained by cardiac failure or fluid overload. By defining the cause of ARDS, one can potentially lessen the effects and time course of the disease with treatment of the underlying cause. While infection or trauma is the traditional cause, solutions used for wound/ mouth care are often under identified as a potential toxin. The case of W demonstrates how the use of a common and seemingly innocent betadine solution caused severe respiratory injury and compromise.
CASE PRESENTATION: W is a 47 year-old male with history of hypertension who presented after 2 weeks of influenza like illness. He quickly developed respiratory distress, hemoptysis, and airway compromise leading to emergent nasal intubation. Further investigation revealed history of recent tooth extraction with a CT scan showing probable necrotizing fasciitis of the retropharyngeal space. He received prompt and appropriate antibiotics, fluid, and vasopressors while awaiting surgical evaluation. On exam, W was nasally intubated in no distress and able to answer questions. His ABG at the time showed 7.402/39.7/60.1/24.2 on 40%. The only significant finding aside from fever was stridor despite the nasotracheal tube in place. W was taken to surgery for tracheostomy, neck washout and debridement revealing edematous tissue and dirty dishwater nonpurulent fluid in the retropharyngeal space. Drains were placed in the neck with plans for irrigation twice daily with betadine solution. Three days later, W had an acute respiratory decompensation from CPAP 60% to APRV 100%. W remained afebrile and normotensive during this time. ABG revealed new hypoxia 7.362/48/63/26.6. Chest radiograph demonstrated new bilateral infiltrates and on exam a frothy brown secretion from the tracheostomy had developed. While W was being treated with standard of care in the ICU including antibiotics and investigation of possible new sites of infection an answer could not be found. A hypothesis was presented that the betadine was somehow leaking into his tracheostomy which led to his respiratory distress. The irrigation was switched to saline and within 24 hours the patient showed drastic improvement in his ventilator requirements to PS 60% with ABG of 7.337/49.9/94.4/26.1. Antibiotics were narrowed to cover only group A streptococcus. Within 48 hours oxygen requirements were down to 40% FiO2 and an ABG of 7.425/39.1/91/25. Within 5 days he was on tracheostomy collar trials and by the end of the month was discharged from the hospital without a tracheostomy or supplemental oxygen.
DISCUSSION: There is scant literature of betadine pulmonary toxicity leading to ARDS. While small in number, the evidence is quite striking to support a cause and effect relationship of topical toxicity. In the case reports found, the presentation occurred when the solution was used to clean/disinfect the mouth and throat in head-neck surgery. All cases had sudden increase in oxygen requirement after the solution was aspirated, an increased need of PEEP with difficulty ventilating, and CXR changes consistent with ARDS. The only research study performed on betadine and lung injury by Cheong Soon et al presented that the injuries could be reproduced and manipulated consistently by dose. On examination of rat lungs, there was macroscopic atelectasis, initial inflammation with edema, alveolar rupture and leukocyte infiltration into the interstitium leading to parenchyma loss and finally resolved with scar tissue.
CONCLUSIONS: Betadine is under recognized as a toxic solution as it is so frequently used to sterilize tissues however there are risks with every step one takes in medicine. Unlikely sources of disease are still possible in the art of medicine and as one broadens the possibilities a once unanswerable question becomes easily explained. For W, this theory of betadine pulmonary toxicity became reality and his life and lungs were spared.
Reference #1: Cheong Soon et al. Lung injury induced by the pulmonary instillation of providone-iodine in rats. J anesthesia (2012) 26:70-79
Reference #2: Tae Hun An, Byung Ryang Ahn. Pneumonia due to aspiration of povidine iodine after induction of general anesthesia. Korean J Anesthesiology 2011. September 61(3): 251-256
Reference #3: Chepla Kyle, Gosain Arun. Interstitial pneumonitis after betadine aspiration. The journal of craniofacial surgery 23(6). November 2012
DISCLOSURE: The following authors have nothing to disclose: Jennifer Osborne
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